WNK4 Polyclonal Antibody

catalytic activity:ATP + a protein = ADP + a phosphoprotein.,caution:Cys-203 is present instead of the conserved Lys which is expected to be an active site residue. Lys-186 appears to fulfill the required catalytic function.,cofactor:Magnesium.,disease:Defects in WNK4 are a cause of pseudohypoaldosteronism type II (PHAII) [MIM:145260]. PHAII is an autosomal dominant disease characterized by severe hypertension, hyperkalemia, and sensitivity to thiazide diuretics which may result from a chloride shunt in the renal distal nephron.,enzyme regulation:Activation requires autophosphorylation of Ser-335. Phosphorylation of Ser-331 also promotes increased activity.,function:Regulates the activity of the thiazide-sensitive Na-Cl cotransporter, SLC12A3, by phosphorylation which appears to prevent membrane trafficking of SLC12A3. Also inhibits the renal K(+) channel, KCNJ1, via a kinase-independent mechanism by which it induces clearance of the protein from the cell surface by clathrin-dependent endocytosis. WNK4 appears to act as a molecular switch that can vary the balance between NaCl reabsorption and K(+) secretion to maintain integrated homeostasis.,similarity:Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. WNK subfamily.,similarity:Contains 1 protein kinase domain.,subcellular location:Present exclusively in intercellular junctions in the distal convoluted tubule and in both the cytoplasm and intercellular junctions in the cortical collecting duct. WNK4 is part of the tight junction complex.,subunit:Interacts with the C-terminal region of KCNJ1.,tissue specificity:Expressed in kidney, colon and skin.,